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bFGF rescues imatinib/STI571-induced apoptosis of sis-NIH3T3 fibroblasts.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology. (Botling)
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2009 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 381, no 2, 165-170 p.Article in journal (Refereed) Published
Abstract [en]

PDGF-B-transfected, sis-NIH3T3 fibroblasts serve as a model system for examining the role of PDGF signaling in tumors. We have found that imatinib/STI571, a tyrosine kinase inhibitor targeting PDGF receptors, induces apoptosis of sis-NIH3T3 fibroblasts cultured under serum free conditions, which was rescued by the addition of 10% newborn calf serum (NCS). Therefore, growth factors included in serum were tested with regard to their ability to rescue imatinib-induced apoptosis. While PDGF-AB, EGF, and IGF-I failed to protect imatinib-induced sis-NIH3T3 cell apoptosis, bFGF rescued it. The effects of bFGF were confirmed by both cell viability assays and Bax/Bcl-2 gene expression ratio. An FGF receptor inhibitor, PD166866, invalidated the protective effect of bFGF. However, combination of imatinib and PD166866 failed to induce cell death of sis-NIH3T3 cells when cultured in 10% NCS. These results indicate that synergistic administration of some types of tyrosine kinase inhibitors need to be tested under in vivo-like conditions to establish novel strategies in anti-cancer therapy.

Place, publisher, year, edition, pages
2009. Vol. 381, no 2, 165-170 p.
National Category
Medical Genetics Cell and Molecular Biology
Research subject
Molecular Medicine; Pathology
URN: urn:nbn:se:uu:diva-125854DOI: 10.1016/j.bbrc.2009.02.012ISI: 000264455900007PubMedID: 19338769OAI: oai:DiVA.org:uu-125854DiVA: diva2:321092
Available from: 2010-05-28 Created: 2010-05-28 Last updated: 2010-07-13Bibliographically approved

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